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表没食子儿茶素没食子酸酯:解析其保护机制与治疗潜力

Epigallocatechin-Gallate: Unraveling Its Protective Mechanisms and Therapeutic Potential.

作者信息

Dong Xiang-Wen, Fang Wen-Lan, Li Yun-Hang, Chai Yu-Rong

机构信息

School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, People's Republic of China.

The First Clinical Medical School, Zhengzhou University, Zhengzhou, Henan, People's Republic of China.

出版信息

Cell Biochem Funct. 2025 Feb;43(2):e70056. doi: 10.1002/cbf.70056.

DOI:10.1002/cbf.70056
PMID:39915982
Abstract

Epigallocatechin-gallate (EGCG), the predominant catechin in green tea, is a key constituent of tea polyphenols. Due to the EGCG's diverse biological activities of anti-inflammatory, antioxidant, and so forth, green tea is believed to exert a positive influence on a variety of diseases. And extensive research had uncovered a range of protective effects attributed to EGCG, indicating its potential to mitigate various pathological conditions. The precise mechanisms through which EGCG operates remain a subject of ongoing discussion among researchers. Reactive oxygen species (ROS), a primary culprit in oxidative stress, have been demonstrated to be reduced by EGCG. Furthermore, nuclear factor kappa-B (NF-κB), a pivotal signal molecular of inflammation progress, has been observed to be suppressed by EGCG. Sirtuins1 (Sirt1) is a histone deacetylase, the obligate substrate of which is NAD+. Evidence suggests that EGCG can enhance the activities of Sirt1 to induce autophagy to protect inflammation injury and oxidative stress in tissues and organs. Despite the promising protective effects of EGCG, its clinical use is constrained by its limited bioavailability. This review aims to consolidate the existing evidence and elucidate the mechanisms that support EGCG's protective role, as well as to explore the challenges and potential strategies for its clinical application.

摘要

表没食子儿茶素没食子酸酯(EGCG)是绿茶中的主要儿茶素,是茶多酚的关键成分。由于EGCG具有抗炎、抗氧化等多种生物活性,绿茶被认为对多种疾病具有积极影响。广泛的研究发现了一系列归因于EGCG的保护作用,表明其具有减轻各种病理状况的潜力。EGCG发挥作用的确切机制仍是研究人员持续讨论的主题。活性氧(ROS)是氧化应激的主要元凶,已证明EGCG可使其减少。此外,核因子κB(NF-κB)是炎症进展的关键信号分子,已观察到EGCG可对其产生抑制作用。沉默调节蛋白1(Sirt1)是一种组蛋白脱乙酰酶,其专一性底物是NAD+。有证据表明,EGCG可增强Sirt1的活性,以诱导自噬,从而保护组织和器官免受炎症损伤和氧化应激。尽管EGCG具有令人期待的保护作用,但其临床应用受到其有限的生物利用度的限制。本综述旨在整合现有证据,阐明支持EGCG保护作用的机制,并探讨其临床应用面临的挑战和潜在策略。

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